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Articles in PresS, published online ahead of print March 18, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00351.2001
Submitted on November 27, 2001
Accepted on March 14, 2002
1 Department of Physiology, Vascular Biology Center, Medical College of Georgia, Augusta, GA, USA; Physiology, Tulane University, New Orleans, LA, USA
2 Department of Medicine (Nephrology) and Molecular Biology & Biophysics, Vanderbilt University School of Medicine, Nashville, TN, USA
3 Departments of Medicine (Nephrology) & Pharmacology, Vanderbilt University School of Medicine, Nashville, TN, USA
* To whom correspondence should be addressed. E-mail: jdimig{at}mail.mcg.edu.
The current studies were performed to determine the contribution of EP2 receptors to renal hemodynamics by examining afferent arteriolar responses to PGE2, butaprost, sulprostone and endothelin-1 in EP2 receptor deficient male mice (EP2-/-). Afferent arteriolar diameters averaged 17.8 ± 0.8 µm in wild-type (EP2+/+) mice and 16.7 ± 0.7 µm in EP2-/- mice at a renal perfusion pressure of 100 mm Hg. Vessels from both groups of mice responded to norepinephrine (0.5 µM) with similar 17-19% decreases in diameter. Diameters of norepinephrine preconstricted afferent arterioles increased by 7 ± 2% and 20 ± 6% in EP2+/+ mice in response to 1 µM PGE2 and 1 µM butaprost, respectively. In contrast, afferent arteriolar diameter of EP2-/- mice decreased by 13 ± 3% and 16 ± 6% in response to PGE2 and butaprost. The afferent arteriolar vasoconstriction to butaprost in EP2-/- mice was eliminated by angiotensin converting enzyme inhibition. Sulprostone, an EP1 and EP3 receptor ligand, decreased afferent arteriolar diameter in both groups, however; the vasoconstriction in the EP2-/- mice was greater than in the EP2+/+ mice. Endothelin-1 mediated afferent arteriolar diameter responses were enhanced in EP2-/- mice. Afferent arteriolar diameter decreased by 29 ± 7% in EP2-/- and 12 ± 7% in EP2+/+ mice following administration of 1 nM endothelin-1. These results demonstrate that the EP2 receptor mediates a portion of the PGE2 afferent arteriolar vasodilation and buffers the renal vasoconstrictor responses elicited by EP1 and EP3 receptor activation as well as endothelin-1.
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